scholarly journals Fluctuations in cell proliferation, apoptosis, and cell cycle regulation at the early stage of tumor promotion in rat two-stage carcinogenesis models

2012 ◽  
Vol 37 (6) ◽  
pp. 1113-1126 ◽  
Author(s):  
Eriko Taniai ◽  
Atsunori Yafune ◽  
Masayuki Kimura ◽  
Reiko Morita ◽  
Fumiyuki Nakane ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Regulation ◽  
Early Stage ◽  
Tumor Promotion ◽  
Two Stage ◽  
Cycle Regulation ◽  
Carcinogenesis Models

Disruptive cell cycle regulation involving epigenetic downregulation of Cdkn2a (p16Ink4a) in early-stage liver tumor-promotion facilitating liver cell regeneration in rats

Toxicology ◽  
2012 ◽  
Vol 299 (2-3) ◽  
pp. 146-154 ◽  
Author(s):  
Takuma Tsuchiya ◽  
Liyun Wang ◽  
Atsunori Yafune ◽  
Masayuki Kimura ◽  
Takumi Ohishi ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Liver Cell ◽  
Liver Tumor ◽  
Cell Cycle Regulation ◽  
Early Stage ◽  
Tumor Promotion ◽  
Cell Regeneration ◽  
Cycle Regulation

p205, A potential tumor suppressor, inhibits cell proliferation via multiple pathways of cell cycle regulation

FEBS Letters ◽  
2006 ◽  
Vol 580 (5) ◽  
pp. 1205-1214 ◽  
Author(s):  
Benyam Asefa ◽  
Jonathan M. Dermott ◽  
Philipp Kaldis ◽  
Karen Stefanisko ◽  
David J. Garfinkel ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Tumor Suppressor ◽  
Cell Cycle Regulation ◽  
Cycle Regulation ◽  
Potential Tumor Suppressor

MAGE-C1/CT7 Inhibition Increases Myeloma Cell Line Sensitivity to Bortezomib-Induced Apoptosis: New Target for Myeloma Therapy?

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 1908-1908
Author(s):  
Fabricio de Carvalho ◽  
Erico T. Costa ◽  
Anamaria A. Camargo ◽  
Juliana C. Gregorio ◽  
Cibele Masotti ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Line ◽  
Cell Cycle Regulation ◽  
Myeloma Cell ◽  
Myeloma Cell Line ◽  
Empty Vector ◽  
M Phase ◽  
Induced Apoptosis ◽  
Cycle Regulation

Abstract Abstract 1908 Introduction: MAGE-C1/CT7 encodes for a cancer/testis antigen (CTA) frequently expressed in multiple myeloma (MM) that may be a potential target for immunotherapy in this still incurable disease. The expression of this CTA is restricted to malignant plasma cells and a positive correlation between MAGEC1/CT7 expression and advanced stage has been demonstrated for MM. It has been suggested that MAGE-C1/CT7 might play a pathogenic role in MM; however, the exact function of this protein in the pathophysiology of MM is not yet understood. Objectives: (1) To clarify the role of MAGE-C1/CT7 in the control of cellular proliferation and cell cycle regulation in myeloma cell line SKO-007 and (2) to evaluate the impact of silencing MAGE-C1/CT7 on cells treated with bortezomib. Material and Methods: Short hairpin RNA (shRNA) specific for MAGE-C1/CT7 was inserted in the pRETROSUPER(pRS) retroviral vector. The pRS-shRNA-MAGE-C1/CT7 was co-transfected with pCL-amphotropic packing vector in 293T cells to produce virus particles. Sko-007 myeloma cell line was transduced for stable expression of shRNA-MAGE-C1/CT7. Downregulation of MAGE-C1/CT7 was confirmed by real time PCR (RQ-PCR) and western blot. Functional studies included cell proliferation, cell cycle analysis using propidium iodide, and analysis of apoptosis using annexin V staining. Results: SKO-007 MM cell line was transduced for stable expression of shRNA-MAGE-C1/CT7. SKO-007 cells were divided into three derivatives: empty vector (pRS) and ineffective shRNA (antisense strand deleted – GC bases) [both used as controls for all the experiments] and inhibited (shMAGE-C1/CT7). MAGE-C1/CT7 mRNA expression was ∼5 times lower in inhibited cell line than control cells by RQ-PCR. Western blot showed 70–80% decrease in MAGE-C1/CT7 protein expression in inhibited cells when compared with controls. Functional assays did not indicate a difference in cell proliferation and DNA synthesis when inhibited cells were compared with controls. We used empty vector, ineffective shRNA and inhibited cells to determine whether inhibition of MAGE-C1/CT7 was associated with cell cycle dysregulation. We detected differences between inhibited cells and both controls regarding the proportion of myeloma cells in the G2/M phase (p<0.05). When inhibited cells and controls were treated with 10 nM bortezomib for 48h, inhibited cells showed a 48% reduction of cells in the G2/M phase but control cells have 11% (empty vector) and 10% (ineffective shRNA) of reduction (p<0.05). Inhibited cells treated with 15 nM bortezomib showed an increased percentage of apoptotic cells in comparison with bortezomib treated controls (p<0.01) [Figure]. Conclusions: MAGE-C1/CT7 antigen inhibition did not change cell proliferation and DNA synthesis in SKO-007 cells. However, we found that MAGE-C1/CT7 plays in cell cycle regulation, protecting SKO-007 cells against bortezomib-induced apoptosis. Therefore, MAGE-C1/CT7 silencing by shRNA could be a strategy for future therapies in MM, i.e. in combination with proteasome inhibitors. [Supported by CNPq and LICR] Disclosures: No relevant conflicts of interest to declare.

scholarly journals GPRC5A facilitates cell proliferation through cell cycle regulation and correlates with bone metastasis in prostate cancer

2019 ◽  
Vol 146 (5) ◽  
pp. 1369-1382 ◽  
Author(s):  
Yuichiro Sawada ◽  
Tadahiko Kikugawa ◽  
Hiroyuki Iio ◽  
Iori Sakakibara ◽  
Shuhei Yoshida ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Bone Metastasis ◽  
Cell Cycle Regulation ◽  
Cycle Regulation

scholarly journals Tetrahydrouridine Inhibits Cell Proliferation through Cell Cycle Regulation Regardless of Cytidine Deaminase Expression Levels

PLoS ONE ◽  
2012 ◽  
Vol 7 (5) ◽  
pp. e37424 ◽  
Author(s):  
Naotake Funamizu ◽  
Curtis Ray Lacy ◽  
Kaori Fujita ◽  
Kenei Furukawa ◽  
Takeyuki Misawa ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Regulation ◽  
Cytidine Deaminase ◽  
Expression Levels ◽  
Cycle Regulation

Effects of Silver Nanoparticles and Silver Nitrate on mRNA and microRNA Expression in Human Hepatocellular Carcinoma Cells (HepG2)

2021 ◽  
Vol 21 (11) ◽  
pp. 5414-5428
Author(s):  
Sheau-Fung Thai ◽  
Carlton P. Jones ◽  
Brian L. Robinette ◽  
Hongzu Ren ◽  
Beena Vallanat ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Dna Damage ◽  
Silver Nitrate ◽  
Hepg2 Cells ◽  
Tissue Repair ◽  
Cell Cycle Regulation ◽  
P53 Signaling ◽  
Cycle Regulation

In order to understand toxicity of nano silver, human hepatocellular carcinoma (HepG2) cells were treated either with silver nitrate (AgNO3) or with nano silver capped with glutathione (Ag-S) at various concentration. Differentially expressed genelists for mRNA and microRNA were obtained through Illumina RNA sequencing and DEseq data analyses. Both treatments showed non-linear dose response relationships for mRNA and microRNA. Gene expression analysis showed signaling pathways common to both nano Ag-S and AgNO3, such as cell cycle regulation, DNA damage response and cancer related pathways. But, nano Ag-S caused signaling pathway changes that were not altered by AgNO3 such as NRF2-mediated oxidative stress response inflammation, cell membrane signaling, and cell proliferation. Nano Ag-S also affected p53 signaling, survival, apoptosis, tissue repair, lipid synthesis, angiogenesis, liver fibrosis and tumor development. Several of the pathways affected by nano Ag-S are hypothesized as major contributors to nanotoxicity. MicroRNA target filter analysis revealed additional affected pathways that were not reflected in the mRNA expression response alone, including DNA damage signaling, genomic stability, ROS, cell cycle, ubiquitination, DNA methylation, cell proliferation and fibrosis for AgNO3; and cell cycle regulation, P53 signaling, cell proliferation, survival, apoptosis, tissue repair and so on for nano Ag-S. These pathways may be mediated by microRNA repression of protein translation.Our study clearly showed that the addition of microRNA profiling increased the numbers of signaling pathways discovered that affected by the treatments on HepG2 cells and gave US a better picture of the effects of these reagents in the cells.

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